affinity, because their concentrations are higher than those of the NMDA sites. As
expected, the zinc complexes with lower concentrations and association rates, such
as those formed with the kainate receptors and ATP molecules, are only significant
following the most intense (long) stimulation. It should also be noticed that the
maximum cleft zinc concentration included in the model, 1 μM, does not lead to the
inhibition of N- or L-type VDCCs by zinc, since the threshold, half, and almost full
blockade concentrations are <5, 69, and 150–200 μM, respectively [40, 42]. For all
protocols considered, very small concentrations (in the order of pM-fM) of the
VDCC complexes are formed.
The evaluation of the dynamics of synaptic zinc complexes considered in this
work contributes to a wider knowledge about synaptic zinc changes. Identifying the
main zinc mechanisms involved in mossy fiber zinc clearance is of major importance, considering the potential protective or toxic roles of released zinc at these
highly excitable synapses.
Acknowledgements
M.E. Quinta-Ferreira is grateful to Dr. C.C.A.M. Gielen for providing the conditions to start this work. It was funded by the strategic project UID/NEU/04539/
2013.
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